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This article explores the close link between information exposure and good governance as well as high government institutional performance in light of a special case study of how the Guangdong provincial government and China's central government responded to the outburst of the Severe Acute Respiratory Syndrome (SARS) epidemic in November 2002. It analyzes the possible reasons behind the initial misinformation on the crisis. Also, it analyzes the lessons the Chinese government learned from the event and the mutative character of government behavior toward information exposure after this short SARS episode. In this regard it focuses on several pioneering programs leading to more open government and transparent policy, such as in Guangdong and Shanghai, and emphases the significant importance of public participating for sound policymaking and democratic governance in the country.

Datasets examining periodontal disease records current (disease) status information of tooth‐sites, whose stochastic behavior can be attributed to a multistate system with state occupation determined at a single inspection time. In addition, the tooth‐sites remain clustered within a subject, and the number of available tooth‐sites may be representative of the true periodontal disease status of that subject, leading to an 'informative cluster size' scenario. To provide insulation against incorrect model assumptions, we propose a non‐parametric regression framework to estimate state occupation probabilities at a given time and state exit/entry distributions, utilizing weighted monotonic regression and smoothing techniques. We demonstrate the superior performance of our proposed weighted estimators over the unweighted counterparts via a simulation study and illustrate the methodology using a dataset on periodontal disease.

Bowei Liu,1 Wei Wang,2 Suofeng Sun,1 Hui Ding,1 Ling Lan,1 Xiuling Li,1 Shuangyin Han1 1Department of Gastroenterology, Zhengzhou University People's Hospital (Henan Provincial People's Hospital), Zhengzhou, Henan, 450003, People's Republic of China; 2Department of Gastroenterology, Changhai Hospital, Second Military Medical University/Naval Medical University, Shanghai 200433, People's Republic of ChinaCorrespondence: Shuangyin Han; Xiuling Li Department of GastroenterologyZhengzhou University People's Hospital (Henan Provincial People's Hospital), No. 7, Weiwu Road, Zhengzhou, Henan 450003, People's Republic of ChinaEmail hanshuangyin123@yandex.com; li_xiuling123@126.comBackground: Pancreatic cancer ranks first among the most aggressive malignancies. Long non-coding RNA (LncRNA) ABHD11-AS1 is known to be upregulated in pancreatic cancer. However, the mechanism by which ABHD11-AS1 mediates the tumorigenesis of pancreatic cancer remains unclear.Methods: Gene and protein expressions in pancreatic cancer cells were detected by qRT-PCR and Western blot, respectively. Cell viability was measured by CCK-8 assay. Cell apoptosis and cycle were tested by flow cytometry. In addition, cell migration and invasion were tested by wound healing and transwell assay, respectively. The correlation between ABHD11-AS1, miR-1231 and cyclin E1 was confirmed by dual-luciferase report and RNA pull-down. Finally, xenograft mice model was established to investigate the role of ABDH-AS1 in pancreatic cancer in vivo.Results: ABHD11-AS1 was found to be negatively correlated with the survival rate of patients with pancreatic cancer. ABHD11-AS1 silencing significantly inhibited the proliferation and induced the apoptosis of pancreatic cancer cells. Additionally, knockdown of ABHD11-AS1 greatly inhibited the migration and invasion of pancreatic cancer cells. Meanwhile, ABHD11-AS1 bound to miR-1231 and cyclin E1 was found to be the target of miR-1231. Moreover, ABHD11-AS1 knockdown-induced G1 arrest in pancreatic cancer cells was reversed by miR-1231 antagomir. Finally, knockdown of ABHD11-AS1 obviously inhibited the tumor growth of pancreatic cancer in vivo.Conclusion: ABHD11-AS1 silencing significantly inhibited the tumorigenesis of pancreatic cancer in vitro and in vivo. Thus, ABHD11-AS1 may serve as a potential target for the treatment of pancreatic cancer.Keywords: pancreatic cancer, ABHD11-AS1, miR-1231, cyclin E1

Wei Wang,1,* Bowei Liu,2,* Suofeng Sun,2 Ling Lan,2 Yu Chen,3 Shuangyin Han,2 Xiuling Li,2 Zhaoshen Li1 1Department of Gastroenterology, Changhai Hospital, Second Military Medical University/Naval Medical University, Shanghai 200433, People's Republic of China; 2Department of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan 450003, People's Republic of China; 3Department of Gastroenterology, Nanhai Hospital, Southern Medical University, Foshan, Guangdong 528200, People's Republic of China*These authors contributed equally to this workCorrespondence: Xiuling LiDepartment of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, No. 7 Weiwu Road, Jinshui District, Zhengzhou, Henan 450003, People's Republic of ChinaTel +86-371-65580014Email li_xiuling123@126.comBackground: 5-Fluorouracil (5-Fu) has been applied to treat pancreatic cancer, which is one of the most common types of digestive system tumors. Evidence has shown that miR-486-5p could promote the proliferation of pancreatic cancer cells. Therefore, this study aimed to investigate whether downregulation of miR-486-5p could enhance the anti-tumor effect of 5-Fu on pancreatic cancer cells.Methods: Cell Counting Kit 8 assay, flow cytometry and wound healing assays were used to detect proliferation, apoptosis and migration in PANC-1 cells. The expressions of Bcl-2, Bax, cleaved caspase 3, PTEN, p-Akt and p-ERK in PANC-1 cells were detected with Western blot assay.Results: In this study, the inhibitory effects of 5-Fu on the proliferation, migration and invasion of PANC-1 cells were significantly enhanced following transfection with miR-486-5p antagonist. In addition, downregulation of miR-486-5p markedly enhanced the pro-apoptosis effect of 5-Fu on PANC-1 cells. Moreover, bioinformatics analysis and luciferase reporter assay identified that PTEN was the directly binding target of miR-486-5p. Meanwhile, downregulation of miR-486-5p markedly enhanced the anti-tumor effect of 5-Fu in PANC-1 cells via upregulation of the level of PTEN, and downregulation of the expressions of p-ERK and p-Akt. In vivo experiments confirmed that knockdown of miR-486-5p could enhance the anti-tumor effect of 5-Fu in PANC-1 xenograft model.Conclusion: We found that the downregulation of miR-486-5p could enhance the anti-tumor effect of 5-Fu on pancreatic cancer cells. Therefore, miR-486-5p antagonist plus 5-Fu might be considered as a potential therapeutic strategy for the treatment of pancreatic cancer.Keywords: pancreatic cancer, 5-fluorouracil, miR-486-5p, PTEN, apoptosis